I thought I was up to speed on this but I still learned new things. I had no idea that nitrous oxide was harmful and even more so if you have certain gene mutations. I have had a lot of dental work and I take nitrous oxide since I dont seem to get numb with the novocaine (slow to numb) and the gas helps me not focus on the pain. There is a lot more in Ben's latest presentation. It went very fast, he is promoting his upcoming MTHFR seminar for Drs. I know I have been sick and at times extremely sick for many years and I appreciate he admonishes Drs that they cant just tell sick patients like us to try this supplement, do this test and see me in 3 months. That has always been my complaint, there is no sense of urgency by so many Drs. Also mentions the methylation cycle has to be restarted/balaced carefully, depending on polymorphisms, otherwise patient can get more sick which is what has happened to me over the years and particularly last year. I am so worn out but I'm still trying not to give up but the medical people that are involved in my case just dont get how hard, how much energy I have used just trying to keep going.

I thought I was up to speed on this but I still learned new things. I had no idea that nitrous oxide was harmful and even more so if you have certain gene mutations. .

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That's for sharing. I get very sick (extremely nauseus immediately if I have it) and actually collapse with nitrous oxide even when they turned it down, I still collapsed with it. Due to my very bad experiences with this over 20 years ago (before I had ME), I havent had it again nor wouldnt. I have a double copy of the Mthfr mutation.

did not realize there might also be a connection t depression with MTHFR, the study linked under depresion only appears to study the 677 MTHFR not the 1298 (I could not see the entire article). I just wonder why are some gnes and SNPs studied more than others? A1298C is suggested often as not meaningful, why do people propogate such views when in actuality there has not been much study done for those with other MTHFR mutations. So to say the other MTHFR mutations are not meaningful seems short sighted and harmful to those who struggle with symptoms and they have no 677 mutation but their other MTHFRs do have mutations. I'm just frustrated, some times I feel as a group we perpetuate the harm when we make judgements with out proof...

did not realize there might also be a connection t depression with MTHFR, the study linked under depresion only appears to study the 677 MTHFR not the 1298 (I could not see the entire article). I just wonder why are some gnes and SNPs studied more than others? A1298C is suggested often as not meaningful, why do people propogate such views when in actuality there has not been much study done for those with other MTHFR mutations. So to say the other MTHFR mutations are not meaningful seems short sighted and harmful to those who struggle with symptoms and they have no 677 mutation but their other MTHFRs do have mutations. I'm just frustrated, some times I feel as a group we perpetuate the harm when we make judgements with out proof...

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Actually there have been studies about the effect of A1298C. And it doesn't do much by itself, but can exacerbate the folate problems of someone who is heterogeneous for C677T. It gets studied less because it's been proven not to have an effect by itself, thus is less interesting. Whereas C677T does have an effect, so researchers want to see how it effects whatever disease/etc that they're interested in.

This is one study about the dangerous elevation of homocysteine when Nitrous Oxide anesthesia is used in those who are homozygous for EITHER C677T or A1298C. I can only find the abstract which doesn't indicate whether the effect of one is greater than the other but both are important by themselves.

The fact that A1298C has less or no effect by itself in some of the things that C677T has a large effect doesn't make it not worth studying.

"OBJECTIVE: To determine associations of methotrexate (MTX) efficacy and toxicity with single-nucleotide polymorphisms (SNPs) in genes coding for folate pathway enzymes in patients with early rheumatoid arthritis (RA).

CONCLUSION: Patients with MTHFR 1298AA and MTHFR 677CC showed greater clinical improvement with MTX, whereas only the MTHFR 1298C allele was associated with toxicity. In the future, MTHFR genotypes may help determine which patients will benefit most from MTX treatment.

There's also a HUGE range of responses to the gassing, with the median far lower than the max - which suggests that a couple outliers dragged the average up. As they discuss in the paper, these results could be due to the small sample sizes in the wild-homozygous and homozygous-wild groups, and/or it seems likely that there is another unknown factor affecting results to a greater extent.

The full text of the 2nd one is at http://onlinelibrary.wiley.com/doi/10.1002/art.21726/pdf
That one is looking at the effect of drug treatments, so again is not looking at the standard functioning of the SNPs, but rather how they might impact the RA patients' reactions to a drug.

I think this one is a bad study. To start with, it's being funded by insurance companies. It also uses subjective outcomes to determine improvement (sounds familiar), and is not talking about folate or even B12 or homocysteine status at all. It's also uncontrolled, so placebo effect could be a big factor. They report lab results from the beginning of the trial, but none from the end - did they not measure them at the end, or are they trying to hide objective data which contradicts the subjective outcome?